Introduction to Heart Conduction and ECG
This lecture by Dr. EM Anvarasi provides an in-depth overview of the heart's electrical conduction system, essential for understanding electrocardiography (ECG).
Conducting System of the Heart
- The heart's electrical activity originates from specialized pacemaker cells that trigger mechanical contraction.
- Cardiac cells are classified by function into pacemaker cells (SA node, AV node, Bundle of His, Purkinje fibers) and contractile cells (atrial and ventricular myocytes).
- Based on conduction speed, cells are slow fibers (SA and AV nodes) and fast fibers (Purkinje fibers, atrial and ventricular myocytes).
- The SA node, located in the right atrium, is the primary pacemaker with a rate of 60-100 bpm, generating the normal sinus rhythm.
- The AV node acts as a secondary pacemaker (40-60 bpm) and introduces a critical delay to allow atrial contraction before ventricular contraction.
- The Bundle of His branches into right and left bundles, with the left further dividing into anterior and posterior fascicles, connecting to the Purkinje fiber system.
Pacemaker Activity and Regulation
- Pacemaker potential is a spontaneous, time-dependent depolarization that triggers action potentials at regular intervals.
- The SA node has the fastest intrinsic rate, followed by the AV node and Purkinje fibers.
- Sympathetic stimulation increases heart rate by enhancing calcium channel activity via beta-1 receptors.
- Parasympathetic stimulation decreases heart rate by increasing potassium conductance and delaying calcium channel opening via M2 receptors.
Cardiac Muscle Structure and Electrical Coupling
- Cardiac muscle cells are striated, branched, and connected by intercalated discs containing desmosomes and gap junctions.
- Gap junctions allow low-resistance electrical current flow, enabling rapid spread of depolarization across myocardial cells.
- The intracellular current flows from excited to resting cells, while extracellular current flows oppositely, generating electrical vectors recorded as ECG.
Cardiac Muscle Properties
- Key properties include excitability (response to stimuli), conductivity (spread of action potential), contractility (force generation), and rhythmicity (automaticity).
- Pacemaker cells exhibit unstable resting membrane potentials with slow depolarization (prepotential) leading to action potentials.
- Contractile cells have stable resting potentials and distinct action potential phases: rapid depolarization (Na+ influx), initial repolarization, plateau (Ca2+ influx), and repolarization (K+ efflux).
Ionic Basis of Pacemaker and Contractile Potentials
- Pacemaker potential involves decreased K+ efflux, funny Na+ channels, and T-type and L-type Ca2+ channels.
- Contractile action potentials rely on voltage-gated Na+ channels for rapid depolarization and Ca2+ channels for plateau phase.
Conduction Velocity and AV Nodal Delay
- SA and AV nodes conduct slowly (~0.05 m/s), while Purkinje fibers conduct rapidly (~4 m/s).
- AV nodal delay (~0.1 seconds) ensures atrial contraction completes before ventricular contraction, optimizing cardiac output.
- Sympathetic stimulation shortens AV nodal delay; parasympathetic stimulation lengthens it.
Spread of Excitation and ECG Correlation
- Excitation begins at the SA node, spreads through atria (P wave), then through the AV node, Bundle of His, and Purkinje fibers to ventricles (QRS complex).
- Ventricular repolarization produces the T wave.
- ECG waveforms represent the sum of electrical vectors from all cardiac tissues at a given time.
Summary
- The heart's conduction system integrates pacemaker and contractile cells with distinct conduction speeds.
- Electrical impulses propagate via gap junctions and specialized pathways, producing characteristic ECG waveforms.
- Understanding these mechanisms is crucial for interpreting ECG and managing cardiac rhythm disorders.
This foundational knowledge sets the stage for advanced ECG analysis and clinical applications.
For a deeper understanding of the heart's anatomy and physiology, check out our article on Comprehensive Heart Anatomy, Physiology, and Electrolyte Balance Explained. To explore the broader context of human physiology, see Understanding Human Physiology: A Comprehensive Overview of the Circulatory System. If you're interested in the electrical principles behind circuits, you might find Understanding Conductors and Capacitors in Electric Circuits helpful. Additionally, for key concepts related to circuits, refer to Understanding Circuits: Key Concepts and Theories. Finally, for insights into electromagnetic principles, check out Comprehensive Guide to Electromagnetic Induction and Inductance Principles.
[Music] [Music] hello everyone
and welcome to this online course on electrocardiogram i am dr em anvarasi professor of
physiology from chetnad hospital and research institute in this very first video lecture we are
going to see about the basic conduction of the heart this is very important in understanding the principles of
electrocardiography in this lecture i am going to take you all through the functional anatomy of the conducting
system of the heart the role of gap junctions the various cardiac potentials namely the pacemaker potential
and the ventricular action potential how this wave of excitation is spread to the entire myocardium and then and there
will be seeing about the control of excitation and conduction in the heart in the first section
we are going to see about the conducting system of the heart this is nothing but the electrical
pathway that lead on to atrial and the ventricular contraction the electrical activity is produced by one group of
cells that leads on to the mechanical phenomenon that is your ventricular muscle contraction
now the cardiac cells are classified based on the function as well as based on the speed of conduction
based on the function the cardiac cells are classified as pacemaker cells and contractile cells
the sa node av node bundle of his and its branches and the purkinje fiber system forms the pacemaker cells whereas
the adrenal and the ventricular cardiac myocytes form the contractile cells based on the speed of conduction the
cardiac cells are classified as slow fibers and fast fibers the sa node and the av node are the slow fibers whereas
the purkinje fiber system atrial and the ventricular myocytes are the fast conducting fibers
in this picture we are seeing the conducting system of the heart you can see here this is a structure
present in the roof of the right atrium this is the sa node there is another structure in the floor
of the right atrium which is called as a a b node these two structures are
ah connected to each other by means of three inter nodal tracks the anterior middle and the posterior inter nodal
tract also a branch of the anterior internal tract also goes to the left atrium to excite the left atrium
the av node continues as his bundle which very soon branches into right branch and the left branch
the left branch again branches into anterior fascicle and the posterior fascicle both the branches they go and
merge with the purkinje fiber system this is the conducting system of the heart now let us see the pacemakers of
the heart what is the space making activity this is nothing but the spontaneous time
dependent depolarization of the cell membrane that may lead on to an action potential in an otherwise question
resting cell the word time dependent is very important here because this depolarization occurs at a regular
intervals and this regular interval or spacing is the one which is deciding the rhythm of the heartbeat
now there are different cells pacemaker cells in the heart the fastest pacemaker is usually this usually setting the
heart rate the fastest pacemaker is the one which has got the highest frequency so in that order if we can see the sa
node the cyanoatrial node has got the frequency of 60 to 100 beats per minute this is the primary pacemaker of the
heart next is the av node has got the frequency of 40 to 60 beats per minute
which is followed by the purkinje fibers which is capable of producing the electrical activity at a rate of 20 to
40 beats per minute let us see the cyanoatrial node it is located at the wall of the right
atrium just below and to the right of the opening of superior vena cava when compared to the entire heart this
sa node forms the smallest electrical region but this has got the fastest pacemaking activity at a rate of 60 to
100 beats per minute the rhythm produced by the sa node is called as normal sinus rhythm
now this inherent or intrinsic pacemaker activity also called as auto automaticity or auto rhythmicity is
subjected to sympathetic and parasympathetic uh
influence the sympathetic activity increases the automaticity
by acting on the beta receptors whereas the parasympathetic activity decreases the sa nodal activity by acting on the
muscarinic 2 that is m 2 receptors also this sa nodal cells are the targets for the therapeutic agents which try to
modulate the heart rhythm for example the calcium channel blockers beta adrenergic blockers act on the channels
present in these essay noodle cells to modulate the heart rate next we will see about the inter nodal
tracts of impulse conduction as we saw in the previous picture the sa node generates the pacemaker potentials which
will be carried to the av node via these three internodal tracks the anterior or backman's middle or winky back posterior
or thorals bundle apart from that a branch of bachmann's bundle also reaches the left atrium to
excite the left atrial tissues now apart from these physiological inter nodal tracts the general excitation can
also spread from cell to cell in the atrium via a specialized structure called as a gap junctions next in the
order of conducting system is the atrioventricular node which is located in the antero inferior part of the
interaterial septum above the opening of coronary sinus this particular area is called as triangle of koch
compared to the sa node this av node has got fewer pacemaker cells and this also continues as the bundle of
his the main function of this av node is that it acts as a reserve pacemaker that
is when the sa node fails this av node will take up its position of pacemaker
and this conducts the action potential from the atria to the ventricles in an unidirectional way
this also mediates a very important phenomenon called as av nodal delay which will be discussing shortly next
the av node continues as the bundle of his and which merges into the purkinje
system of fibers this bundle of his branch into right branch and the left branch
the left branch once again branch into anterior fascicle and posterior inferior fascicle
the right branch supplies the entire right ventricle whereas the anterosuperior fascicle supplies the
anterior wall of the left ventricle and posterior inferior fascicle supplies the posterior wall of the left ventricle
in the next section we are going to see about the cardiac muscle and its properties like skeletal muscle cardiac
muscle is also a striated muscle with nucleus and many active mitochondria but then the cardiac cells they branch and
interdigitate the most important feature of the cardiac muscle is that the adjacent
cardiac muscles they are united by means of a special structure called as intercalated this this is the
intercalated disc see this is the histological picture of the cardiac muscle the adjacent muscles
when you expand here you can see the adjacent plasma membrane plasma membrane of the adjacent cardiac
cells they approximate each other and forming the specialized structure called as intercalated
disc now when the sa node is generating the action potential the wave of
depolarization is spread from one cell to another via the intercalated disc you can see the intercalated disc is
actually the plasma membrane they which lie in close proximity with the adjacent cells plasma membrane they
are bound tightly with by means of this desmosomes this is the desmosome okay and then in the area where the plasma
membranes approximate each other there is a special channel called as gap junctions which are the low resistance
bridges across which the electrical current flow from one cell to another cell
consider the cells a b c and d are all the adjacent myocardial cells bound to each other by means of this gap
junctions this yellow structure okay and you can see the cells are all in the
resting stage as is denoted by the negative ions lining the interior of the cell while positive ions are lining the
exterior of the cell there are membrane channels present in the cells which can conduct the positive
ions now when the cell a is excited what happens a wave of depolarization will spread from a to b
this will cause increase in the positivity in the cell b which will open up the membrane channels and positive
ions flow into the cell b this will further enhance the positivity or depolarization in the cell b which will
be conducted from b to c by other cap junctions okay and the cell c will now have
increased depolarization in it this wave of current of depolarization from b to c is called as intracellular
current now the same intracellular current will flow from cell c to cell d not only it goes in that direction but
it also displaces some of the positive ions attached to the cell membrane in the cell d and that is called as
capacitance current now this positive ions will flow from cell c back to cell b
in the opposite direction this is called as extracellular current so whenever there is an intracellular
current flowing from one cell to another an equivalent and opposite extracellular current will be flowing in the reverse
direction the flow of this extracellular current in the heart gives rise to an
instantaneous vector in the heart and this changes with time
ecg is nothing but the sum of all these electrical vectors which are recorded at one particular plane at and at one
particular time so the cardiac muscle fibers are actually they connected to each other in series and parallel
their membranes form the intercalated disc which has got the gap junctions across which the current freely flows
from one cell to another in one direction and hence when one cell is excited the action potential can easily
spread through the gap junctions that's how when one cardiac cell is excited the
entire cardiac muscle will act like a sensitive and you ah that is in a unitary
fashion okay in fact we have got one atrial sensitium and one ventricular sensitium that is the importance of this
gap junctions coming to the properties of the cardiac muscle
they are excitability or pathotropism conductivity or dromotropism contractility or ionotropism and
rhythmicity or chronotropism along with that we have got a special feature of refractory period now with respect to
ecg the first two properties that is the excitability and conductivity are very important and we will discuss about that
excitability is nothing but the ability of the cardiac tissue to respond to stimuli by producing an action potential
so in that way there are two types of cardiac tissues excitable cardiac tissues which are conducting tissue
which is producing a pacemaker potential example is the sa node other one is a contractile tissue which produces a true
action potential as seen in the ventricular myocardium what is the space maker potential here
spontaneous time dependent depolarization occurs but the pacemaker cells
show an unstable resting membrane potential the resting membrane potential ranges from minus 65 to minus 55
millivolts now why this resting membrane potential is unstable because there is slow rise of the resting membrane
potential because of the slow depolarization this rising phase of the resting membrane potential is called as
pre potential so when it rises slowly and when it reaches minus 40 millivolts this is the
firing level a rapid depolarization will occur which goes up to plus 5 millivolts which will be followed by rapid d
repolarization this completes one action potential in a pacemaker tissue you can see here
in this picture sa nodal potential is depicted you can see the slope of rising depolarization
from minus 60 gradually it goes up to minus 40 when it reaches minus 40 that is at firing level it
it throws and depolarization which will be followed by a repolarization and again the resting membrane potential is
unstable it keeps on increasing until it reaches the next level next cycle that is mine minus 40 millivolts
the same similar picture is shown in the av node now this slow rise in the depolarization
is called as prepotential what is the ionic basis of this prepotential this happens at the end of repolarization or
sometimes hyper polarization that is why it is called as ih that is hyper polarizing currents now what happens
during the first half or early phases of this prepotential the potassium efflux is decreased the conductance of the
potassium through the potassium channels it is decreased also there are opening up of one particular type of channels
called as leaky sodium channels or the it is otherwise called as funny channels because it allows both the sodium ions
and potassium ions so because of that there is slow entry of the positive ion may be sodium ion that leads to slow
rise in the depolarization the later half of the pre potential is because of opening up of
transient type of calcium channels and calcium influx once it reaches minus 40 millivolts another type of calcium
channels is open that is long lasting calcium channels and there will be rapid inflow of calcium ions remember
the sa nodal potential and the av nodal potential the depolarization is because of opening up of calcium channels sodium
channels has no role in pacemaker potential so the unstable rmp the early part is
due to the hyper polarizing currents as well as the funny currents and the later part is
because of t type calcium channels rapid depolarization is because of
l-type calcium channels and repolarization is because of potassium efflux
look at this picture which shows the regulation of the pacemaker activity by then sympathetic and parasympathetic
activation see this is the normal rhythm of the pacemaker tissue when there is sympathetic stimulation
look at the slope of this prepotential it is increased now why this occurs is the non-adrenaline
produced in the sympathetic nerves they act via the beta 1 receptors it increases the intra cellular cyclic amp
this will open up the l-type calcium channels so rapidly this depolarization will take place that is why it in the
slope is increased okay and the heart rate is also increased now look at the vehicle stimulation look at the slope
here slope of the pre potential is decreased here the acetyl colon released at the vehicle nerves increases the
potassium conductance and slows the hyperpolarizing currents also why are the m2 receptors it delays the opening
up of the calcium channels so that's how it delays the next impulse so this decreases the slope of the prepotential
and hence decreases the heart rate next we will see about the contractile tissue potential see the atrial muscle
as well as the ventricular muscle the one important feature that you should notice is look at the resting
membrane potential it is a stable resting membrane potential ranging from minus 85 to minus 90
millivolts okay so it is the baseline is a straight line it is not a slope unlike in we saw in the pacemaker potential
which will be followed by a rapid rise or a straight depolarization which causes zero
potential and then there will be a small short repolarization which is which followed by a plateau and
then a regular repolarization occurs until it reaches the resting membrane potential
level now this purkinje fiber is
almost similar to the ventricular muscle in terms of the electrical activity but the only is look at the resting membrane
potential this is a pacemaker tissue so this shows the unstable resting membrane potential you
can see the slope whereas in ventricular muscle it is stable it is a straight line here
but similar to the ventricular muscle this has also got a straight line denoting the depolarization that is
rapid depolarization an initial rapid repolarization followed by a plateau and then the slow repolarization this is
because in purkinje fibers the depolarization involves both the sodium channels as
well as the calcium channels whereas in the pacemaker tissue the depolarization is only because of the calcium channels
so the contractile tissue action potential is created by the fast fibers especially the ventricular and the
atrial fibers resting membrane potential is stable and it has got various phases as is
depicted in this picture phase 0 is the rapid depolarization this is because of the sodium
currents and phase 1 will be the initial rapid repolarization this is because of the
closure of the sodium channels as well as opening up of the calcium channels there will be
a plato phase that is phase two which is done by the slow influx of the calcium ions which
will be followed by the repolarization phase 3 and back to the resting membrane potential phase 4 summary of the ionic
basis of cardiac action potential phase 0 is because of the sodium influx through the voltage-gated sodium
channels there will be some influx of calcium ions via the slow calcium sodium channels also phase one will be because
of closure of the sodium channels and opening up of specific type of potassium channels called as i
t o that is transient outward currents of potassium phase two is because of the slow influx
of the calcium channels through the calcium ions through the calcium channels and also slow effects of the
potassium ion so the membrane potential does not change it remains a plateau phase 3 and phase 4 is because of the
efflux of the potassium ions through various types of potassium channels the next important property is that the
conductivity this is nothing but the ability to conduct an action potential by sequential depolarization of the
adjacencies how the action potential is connected from one cell to another almost all the cells are capable of this
property that is conductivity only that the conduction velocity differs for example the sa node and the av node are
the slowest conducting fibers with a velocity of 0.05 meter per second purkinje fiber system is the fastest
conducting system in the heart with a velocity of 4 meter per second atrium ventricle and bundle of his they
conduct at a velocity of 1 meter per second this is the conduction pathway as we all
know sa node generates the potential it transmits to the av node via the internodal tract
to the right atrium and via a branch of internodal anterior interneural tract to the left atrium so within this point one
second the entire right atrium and the left atrium is excited okay and then when the impulse come to the av node
there will be a delay of about point one second in the av node then the node the impulses crosses the
av node goes to the bundle office its branches and then reaches the purkinje system to exit the entire ventricular
myocardium so this takes around point zero eight to point one second so within approximately point three second the
entire heart atria and the ventricle gets excited once the pacemaker potential is generated now what is this
av nodal delay this is one important phenomenon happening in the av node here the conduction of the rapid impulses
will be delayed for about 0.1 second in the av node this is called as detrimental contraction
the reason for this delay is that the transitional fibers which connect the internodal tracks to the av node are
very small and they have very ah slow conduction velocity even less than the sa node and the av node say for
example point zero two to point zero five meter per second and they also have very few gap
junctions we know that the atria and the ventricle are separated by a fibrous ring of tissue and this av node and the
bundle office and its branches are the only way to transmit the impulses okay and the advantage of this av nodal delay
is that because of this delay only the atrium is able to completely contract and empty its blood into the ventricle
before the ventricular contraction stops a sufficient amount of cardiac output is possible only because of this av nodal
delay now this av nodal delay is also shortened by the sympathetic stimulation and lengthened by the parasympathetic
stimulation so once again this picture showing the sa node av node
conduction occurs through the internal tracks and from the av node bundle of is
continues it runs for a short distance in the septum upper part of the septum divides
into right branch and the left branch the left branch again divides into anterior fascicle and the posterior
fascicle and both the branches run down the septum and merges with with the purkinje fiber system now how this
excitation wave spreads we will see in this picture this is the beginning of the atrial
excitation which is the excitation produced in the sa node is travelling towards the av node and in this picture
as shown in this yellowish coloration both the right atrium and the left atrium is
ah excited that means excitation atrial excitation is complete you can see the recording of this action potential
here in the bottom picture when the atrium started its impulse generation a slight upward
deflection has started and when both the atrium are conducted there is a complete one positive wave this wave is the p
wave of ecg next the ventricle is getting excited so when the impulse comes to the bundle of
this which is present in the top of the septum it goes towards the left side little bit
and then in the middle of the septum it turns towards the right side and the spread of excitation goes downwards
towards the apex of the ventricle and then turns upwards on either side towards the av growth
so that's how the complete ventricular myocardium gets excited you can see during the septal activation there is a
formation of some negative wave which will be followed by a positive wave and then when the ventricular excitation is
complete you can see three waveforms q wave r wave and s wave together we call it as
qrs complex that is denoting the ventricular excitation this excitation spreads from endocardium to epicardium
that is very important now next is the ventricular relaxation which is occurring from epicardium to endocardium
and that forms another positive wave called as t wave so once the depolarization comes to the
av node and goes to the bundle office it starts at the left side of the septum and moves to the right across the mid
portion of the septum then the excitation spreads down the septum to the apex and turns
along the walls of the ventricles on both sides right and left side and goes towards the av grow from the endocardium
to the epicardial surface the last portion of the vent of the heart to get excited is the posterior basal portion
of the left ventricle the pulmonary conus and the uppermost part of the septum this is how the spread of
excitation takes place so this is a picture showing the depolarization or the action potential
produced different parts of the conducting system so this is the sa nodal potential you can see here then is
the atrial muscle then the av node then the his bundle its branches
purkinje fiber system finally the ventricular muscle now ecg is nothing but the sum of all
these action potential at any given time on any given plane so this electrical vector of all the action potentials
produced in different conducting systems of the heart gives rise to ecg and its various waveforms namely p wave qrs
complex t wave and uv summarizing the entire content we have seen that the conducting system
of the heart includes the cardiac cells classified as different ways based on the function as pacemaker cells and the
contractile cells and based on the speed of conduction as slow fibers and fast fibers pacemaker cells are sa node av
node bundle office branches purkinje fibers contractile cells or atrial and the ventricular myocytes slow fibers or
sa node and av node whereas other cells are fast fibers next we saw about the production of this
extracellular current that is when the action potential or when the wave of depolarization spreads
from one cell to another cell as intracellular current an equivalent wave of depolarization will spread in
the opposite direction this forms the extracellular electrical vector and the ecg is nothing but sum of all these
electrical vectors recorded at one particular plane at one particular point
and we saw that the conduction pathway is complete within 0.3 seconds since its origin at sa node and there is a delay
of this 0.1 second in the av node which is actually beneficial for producing a better cardiac output
and better contraction now we also saw that how the wave of excitation spreads across the different parts of the
conducting tissue starting from the sa node and then the entire atrium right and the left atrium
gets kind of ah excited that leads on to a positive wave that is p wave then comes the wave of excitation along the
septum and the ventricle muscle and that completes the qrs complex followed by the ventricular relaxation
which gives rise to the t wave this is a picture finally showing the electrical activity that is
depolarization and repolarization pattern in different parts of the conducting system right from the sa node
till the ventricular muscle and the sum of all these electrical activity in terms of action potential is recorded as
different waveforms of ecg so we will be discussing about a lot more about ecg in the further lectures i thank our
university chetna academy of research and education and nptel for enabling this course to the viewers
thank you
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